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Cardiovascular, Renal and Peripheral Pharmacology > Contraction and Relaxation > Flashcards

Contraction and Relaxation Flashcards

1
Q

what channels allow the entry of Ca into the cardio myocyte

A

RyR2

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2
Q

where does intracellular Ca get released from?

A

Sarcoplasmic reticulum

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3
Q

where does the Ca bind to

A

troponin C on actin filaments in the sarcomere

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4
Q

how does the heart muscle relax?

A

K channels open

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5
Q

what receptor takes the Ca back into the sarcoplasmic reticulum

A

SERCA2a

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6
Q

what receptor removes Ca from the cell

A

NXC (Na+/Ca2+ exchanger)

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7
Q

how many ryanodine receptor isotypes are there?

A

3

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8
Q

which isotype is found in the heart

A

RyR2

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9
Q

how are RyR2 receptors arranged?

A

clusters

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10
Q

what does activation of the RyR2 clusters cause

A

calcium spark

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11
Q

what can lead to leaky RyRs

A

caffeine

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12
Q

where/what are RyRs

A

Ryanodine receptors (RyRs) are located in the sarcoplasmic/endoplasmic reticulum membrane and are responsible for the release of Ca2+ from intracellular stores during excitation-contraction coupling in both cardiac and skeletal muscle

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13
Q

consequence of a leaky RyR

A

calcium escape from the intracellular stores into the cytosol possibly causing a premature atrial contraction

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14
Q

effect of low [caffeine]

A

increased sensitivity to RyRs to cytosolic Ca2+

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15
Q

What is SERCA2a

A

SERCA is a type P ATPase pump that transports two calcium ions in exchange of the hydrolysis of one ATP molecule, functioning against a calcium gradient to restore luminal ER calcium levels

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16
Q

what activates SERCA2a

A

increased cytosolic Ca

17
Q

what regulates SERCA2a

A

PLN

18
Q

How can PLN activate SERCA2a

A

if high [Ca] AND PLN is phosphorylated itself (on CAMK11 and PKA sites)

19
Q

what is NCX

A

Na/Ca exchanger

20
Q

what drives the NCX

A

increased cytosolic [Na] or [Ca]

21
Q

how can this operate

A

forward or reverse

22
Q

which is the normal direction?

A

forward (Ca x 1 out, Na x 3 in)

23
Q

what activates the forward direction of the NCX

A

increased cytosolic Ca

24
Q

what is an adverse side effect of NCX

A

can cause membrane depolarisation, which triggers DADs in Ca2+ overloaded myocytes

25
Q

how does the forward reaction affect the cytosolic [Ca]

A

decreases it

26
Q

how is Ca2+ homeostasis regulated in the cardiac myocyte

A

sympathetic nervous system

27
Q

4 main phosphorylation sites

A

Cav1.2 (calcium channel)
RyR2 (on SP)
Troponin 1
PLN-mediated SERCA

28
Q

PLN-mediated SERCA can also cause an

A

increase in force contraction

29
Q

EADs can be caused by

A

hyperphosphorylation and enhanced activity of Cav1.2

30
Q

what predominant effect do catecholamines have

A

positive inotropic

31
Q

how do catecholamines have a positive inotropic effect

A

increase [Ca] in the cytosol via PKA mediated phosphorylation of L-VACC and Ca release via RyR2

32
Q

how do catecholamines have a negative inotropic effect

A

increase Ca reuptake into the SR via PKA-mediated phosphorylation of SERCA (the PLB becomes phosphorylated)

33
Q

4 examples of catecholamines that have a positive inotropic effect

A

NA, A, dobutamine, isoprenaline

34
Q

what effect does digoxin have

A

inhibit Na/K ATPase

35
Q

effect of digoxin

A
  • binds to extracellular K+ site competitively, inactivating it,
  • increasing [Na] in the cytoplasm
  • REVERSE mode on NCX
  • more Ca into the cell
  • +ve inotropy
36
Q

over dose of digoxin

A
  • increased Ca in cytoplasm
  • stimulate FORWARD NCX
  • NCX is electrogenic, so more +ve charges enter than exit
  • membrane depolarisation
  • DADs –> arrhythmias
37
Q

levosimendan

A

is a +ve inotrope

Cardiovascular, Renal and Peripheral Pharmacology (13 decks)

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